Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Preconditioning is the most powerful endogenous mechanism, to protect the heart against ischemic damage. Conflicting data are published whether preconditioning can be induced in case of diabetes and the metabolic syndrome, which are clinically very relevant conditions. If preconditioning could be induced consistently and chronically in this population, an important reduction of surgical morbidity and mortality could be reached. In this project we induced hypoxic preconditioning in mice and used cardiac pressure-conductance catheterisation and infarct size as outcome parameters. In the first part, we found that hypoxic preconditioning was capable to reduce infarct size with 40% and preserve the load-independent parameters with 33% after coronary occlusion. A DKO (double knock-out: ob/ob; LDLR-/-) model for the metabolic syndrome developed a larger infarct size and had a reduced contractility. No preconditioning could be induced in this model. To detect the determing factor of the resistance to preconditioning, we used single knock-out models. A comparable preconditioning effect of wild type mice could be induced in the lipoprotein receptor deficient (LDLR-/-) model for dyslipidemia. The leptin deficient (ob/ob) model, characterized by insulin resistance and abdominal obesity had, identically to the DKO model, a larger infarct size. A second window of preconditioning could be induced, although it was less pronounced than the wild type and LDLR-/- model. Insulin resistance and abdominal obesity could be identified as the major factor in the resistance to preconditioning.
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PMID:[The effect of type II diabetes and the metabolic syndrome on cardiac second window preconditioning]. 1916 97

Toll-Like Receptor (TLR) -2 and -4 expression and TLR-induced cytokine response of inflammatory cells are related to atherogenesis and atherosclerotic plaque progression. We examined whether immediate TLR induced changes in CD11b and L-selectin (CD62L) expression are able to discriminate the presence and severity of atherosclerotic disease by exploring single dose whole blood TLR stimulation and detailed dose-response curves. Blood samples were obtained from 125 coronary artery disease (CAD) patients and 28 controls. CD11b and L-selectin expression on CD14+ monocytes was measured after whole blood stimulation with multiple concentrations of the TLR4 ligand LPS (0.01-10 ng/ml) and the TLR2 ligand P3C (0.5-500 ng/ml). Subsequently, dose-response curves were created and the following parameters were calculated: hillslope, EC50, area under the curve (AUC) and delta. These parameters provide information about the maximum response following activation, as well as the minimum trigger required to induce activation and the intensity of the response. CAD patients showed a significantly higher L-selectin, but not CD11b response to TLR ligation than controls after single dose stimulations as well as significant differences in the hillslope and EC50 of the dose-response curves. Within the CAD patient group, dose-response curves of L-selectin showed significant differences in the presence of hypertension, dyslipidemia, coronary occlusion and degree of stenosis, whereas CD11b expression had the strongest discriminating power after single dose stimulation. In conclusion, single dose stimulations and dose-response curves of CD11b and L-selectin expression after TLR stimulation provide diverse but limited information about atherosclerotic disease severity in stable angina patients. However, both single dose stimulation and dose-response curves of LPS-induced L-selectin expression can discriminate between controls and CAD patients.
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PMID:Toll-Like Receptor induced CD11b and L-selectin response in patients with coronary artery disease. 2357 59

A 62-year-old man with a family history of coronary artery disease and a history of smoking, diabetes and dyslipidemia was admitted to our hospital with chest pain from acute myocardial infarction. Emergent coronary angiography was performed with intervention to a mid-right coronary occlusion with drug-eluting stent implantation. Optical coherence tomography (OCT) visualized well-apposed stent struts and no remarkable tissue protrusion, stent underexpansion, malapposition, edge dissection, and hematoma. Immediately after OCT imaging, a coronary angiogram showed a filling defect surrounded by contrast medium at the site of the stented lesion. OCT imaging was performed again and a low backscattering protrusion suggestive of white thrombus in the coronary lumen was clearly visualized in OCT imaging. We performed thrombus aspiration immediately after OCT imaging. Aspirated thrombi were off-white in color. We made a diagnosis of early-onset heparin-induced-thrombocytopenia (HIT) due to thrombus formation within the stent and positive HIT antibodies. OCT in the acute phase of stent thrombosis allowed us to promptly identify the main causative mechanisms of early stent thrombosis.
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PMID:Optical Coherence Tomography Findings in Early Stent Thrombosis by Heparin-Induced Thrombocytopenia. 2781 79